Our primary aim is the development of novel agents capable of counteracting the enhanced tendency for blood platelet adhesion, release and aggregation in persons (1) bearing prosthetic devices, or (2) linked to biomaterials in contact with their blood; the foremost concern being the prevention of accumulations leading to thromboembolic complications. While there is convincing evidence that both acetylation capability and surface activity are factors of prominent significance in the action of antithrombotic compounds, to the best of our knowledge, specific consideration has not been given as yet to the particular advantages derived from optimizing both of these parameters within the framework of a single molecule. We have conceptualized, therefore, platelet adhesion-release-aggregation-inhibiting compounds which, in addition to their acetylating capabilities, possess distinct affinity for optimal interaction with acetylation-sensitive and other target sites on platelet and other biologic surface structures; antithrombotic agents, substantially surpassing that of aspirin, should be attained by means of surface-active features markedly enhancing initiation and consummation of interaction. By virtue of the structural features of our molecular design, the surface-active component is visualized to continue to exert antihemostatic effects distinct from and subsequent to the acetylation process. In addition to generating antiplatelet agents superior in potency as well as in breadth of activity, the compounds should also serve as molecular probes for the characterization of at least some platelet surface or other biologic target sites. The compounds' efficacy will be compared to that of aspirin, in terms of their (1) ability to inhibit platelet retention by N.B.S. certified and conventionally used biomaterial surfaces; (2) ability to inhibit platelet aggregation induced by collagen, thrombin, arachidonic acid, adenosine diphosphate and epinephrine, (3) ability to accumulate at interfaces in a non-specific manner as reflected by surface and interfacial tension measurements; and (4) ability to interact with components of platelet and other biologic surface structures, or with appropriately constituted model compounds, in monomolecular-film systems. In the platelet retention and aggregation studies whole blood and platelet-rich plasma, from human volunteers, will be employed.